The document outlines the classification, causes, and treatment options for hypertension as per the JNC VII report. It details blood pressure categories, drug classifications including diuretics, ACE inhibitors, and calcium channel blockers, and their specific effects on managing hypertension. It also addresses additional considerations for certain patient populations like those with diabetes, heart failure, or in pregnancy.

1. Hypertension

2. JNC VII
• The seventh report of Joint National
Committee (of USA) on prevention, detection,
evaluation and treatment of high BP

3. Classification
Systolic pressure Diastolic pressure
mmHg mmHg
Normal 90–119 60–79
Prehypertension 120–139 80–89
Stage 1 140–159 90–99
Stage 2 ≥160 ≥100
Isolated systolic
hypertension
≥140 <90
Source: American Heart Association (2003).[5]

4. JNC VII
• Individuals older than 50 years are classified
as having hypertension if their blood pressure
is consistently at least 140 mmHg systolic or
90 mmHg diastolic.
• Patients with blood pressures higher than
130/80 mmHg with concomitant presence of
diabetes mellitus or kidney disease require
further treatment.[5]

5. Etiology
• Essential hypertension
• Family history
• Environmental Factors:
– Stress
– Obesity
– High sodium diet
– Smoking

6. Regulation
• CO X PVR
• Physiologically maintained by moment to
moment regulation of the above product
exerted at: Arterioles, postcapillary venules,
the heart and the kidneys

7. Regulation
• Baro-receptors and the Sympathetic Nervous
System:
– Carotid baro receptors: Stimulated by stretching of the
blood vessel wall by internal BP
– Normally send inhibitory impulses to the vasomotor
centre (VMC)
– Fall in BP causes carotid baro receptors to send fewer
inhibitory impulses to the VMC increasing sympathetic
activity to the heart ( CO) as well as arteriolar
vasoconstriction and vasoconstriction of venules

8. Regulation
• venous return, thus leads to restoration of
normal BP
• The baro-reflex acts in response to:
a. Changes in posture
b. in PVR due to secondary vasodilators
c. intravascular volume due to low sodium diet,
diuretics, blood loss and CCF

9. Regulation
• Renin- Angiotensin System:
• By controlling blood volume, the kidney is responsible
for long term BP control. Occurs through:
• Renal perfusion pressure renal salt & water re
absorption
• Pressure in renal arterioles renin. This results
in the formation of angiotensin II
vasoconstriction, NE & secretion of aldosterone
BP

10. Classification of Drugs
Diuretics
Adrenergic receptor antagonists
Adrenergic receptor agonist: Clonidine,
Guanfacine, Methyldopa
ACE (-)s
Renin (-): Aliskiren
Angiotensin II antagonist
Aldosterone antagonists

11. Classification of Drugs
Vasodilators
Centrally acting adrenergic drugs: Clonidine,
Minoxidil, Guanethidine, Methyldopa

12. Diuretics
• Diuretics BP by reducing sodium stores and
reducing blood volume
• Monotherapy in mild-moderate hypertension
• Combined with sympatholytics or vasodilators
in severe hypertension ( salt and water
retention induced by these agents)

13. Diuretics
• Thiazides are diuretics of choice:
– Effective at low doses e.g. hydrochlorothiazide 12.5
mg/day
– Usually combined with spironolactone (potassium)
– May also be combined with ACE and ARBs
– Recommended in elderly
• Loop diuretics are used if there is co-existing:
– Chronic renal failure
– CCF
– Resistance to combination therapy

14. Beta – Adrenoreceptor Blockers
• Effective for all grades
• Do not produce postural hypotension
• Do not produce salt and water retention
• Used in combination with vasodilators in
severe hypertension to prevent reflex
tachycardia
• Recommended in Young non-obese

15. Beta – Adrenoreceptor Blockers
• Propranolol: non-selective β blocker
• Atenolol: Selective β blocker
• Carvedilol: β blocker with additional α1-
blocking effect
• Labetalol: used IV for hypertensive
emergencies

16. Angiotensin Converting Enzyme
Inhibitors
• Reduction of plasma Ang II causing arteriolar
and venular vasodilatation
• Reduction of aldosterone
• Preservation of kinins which are vasodilators
• Also prevents myocardial hypertrophy and
remodeling following myocardial infarction
• Most appropriate for patients with: diabetes,
nephropathy, Left ventricular hypertrophy,
angina, post MI

17. Angiotensin Converting Enzyme
Inhibitors
A. Vascular Effects:
o Reduce PVR
o Natriuresis
o Minimal change in CO or heart rate (do not
induce reflex tachycardia due to blunting of
sympathetic reflexes (Inhibit Ang II-induced NE
release)
o No postural hypotension

18. Angiotensin Converting Enzyme
Inhibitors
B. Cardiac Effects:
– Arteriolar dilatation
– renovascular resistance ( renovascular
vasoconstriction due to Ang II) --- renal blood
flow
– aldosterone secretion
– Venodilatation-- preload (natriuresis and
preload --- filling pressures ---- improved
pulmonary and venous congestion)

19. Angiotensin Converting Enzyme
Inhibitors
– Reversal of ventricular remodelling through:
– In preload and after load
– Preventing the trophic effects on Ang II on
myocytes
– Attenuating aldosterone- induced cardiac fibrosis
C. Cerebral and coronary blood flow is well
maintained

20. Angiotensin Converting Enzyme
Inhibitors
• Advantages:
1.No change in heart rate
2.No metabolic adverse effects:
– Do not alter blood uric acid levels or cholesterol
levels
– Improve glucose tolerance and diabetic
nephropathy
3.Regression of ventricular hypertrophy

21. Angiotensin Converting Enzyme
Inhibitors
• Therapeutic uses:
1.Hypertension:
– Essential hypertension: first line drug as
monotherapy in mild to moderate hypertension or
combined with diuretics, CCBs or β blockers
– Hypertension with diabetes: 1st
choice
– Hypertension with CCF: combined with a diuretic
– High renin hypertension e.g. unilateral renal
artery stenosis

22. Angiotensin Converting Enzyme
Inhibitors
2. CCF:
– Delay progress of heart failure
– Improve quality of life of the patient
3. Following myocardial infarction:
– Start therapy immediately after infarction
– Preserve left ventricular function and
remodeling

23. Angiotensin Converting Enzyme
Inhibitors
• ADRs:
– First dose hypotension (Start with low dose)
– Skin rash
– Persistent dry cough
– Temporary loss of taste
– Proteinuria and nephrotic syndrome in patients
with renal disease
– Neutropenia (Rare but serious)

24. Angiotensin Converting Enzyme
Inhibitors
• Drug Interactions;
• K+ supplements and K+ sparing diuretics---
hyperkalaemia
• NSAIDs ---- antihypertensive effects of ACEIs

25. Angiotensin II Receptor Blockers
(ARBs)
• More complete inhibition of the effect of Ang
II
• No effect on bradykinin metabolism
• losartan
• ADRs:
– Foetopathic
– Severe hypotension in hypovolemic patients
– Hyperkalaemia in patients with renal disease

26. Ca Channel Blockers
• Vascular Effects:
– Relax arterial smooth muscles:
– Dihydropyridines > Verapamil > Diltiazem
• Cardiac Effects:
i. Effect on myocardial contractility:
– All CCBs produce a negative inotropic effect:
– Verapamil > Dilitiazem
– Dihydropyridines relax vascular smooth muscles at
lower concentrations than those required to induce
negative inotropism.

27. Ca Channel Blockers
• This results in reflex sympathetic activation
overcoming their negative inotropic effect
• contractilty & vasodilatation BP work
done by the heart
ii. Effect on AV nodal conduction:
o Verapamil & Diltiazem HR & AV conduction
o Nifedipine has no effect on AV conduction

28. Ca Channel Blockers
• Preferable in elderly hypertensives
• Effective in low renin hypertension (With no
HF and no volume depletion)

29. Vasodilators
I. Hydralazine:
• Molecular mechanism not known
• Used in severe hypertension
• Cannot be used as monotherapy due to
development of tachyphylaxis
• HR CO (has to be combined with β-
blockers)
• Fluid retention (has to be combined with a
diuretic)

30. Vasodilators
II. Minoxidil: Arteriolar dilator
 Opens K+ channels in smooth muscle
membranes
 Alternative to hydralazine when maximal
doses of hydralazine are not effective
 Used in combination with diuretics & β
blockers to avoid tachphylaxis
 Topical minoxidil is used as a hair growth
stimulant in alopecia

31. Vasodilators
III. Na+
nitroprusside:
Sensitive to light: solution is freshly prepared
and covered with opaque foil
Rapidly metabolized by uptake into RBCs with
liberation of cyanide

32. Vasodilators
Toxicity:
• Accumulation of cyanide: metabolic acidosis,
excessive hypotension, arrythmias,
methaemoglobinemia
• Treatment of cyanide toxicity:
hydroxycobalamine & sodium thiosulfate

33. Vasodilators
IV. Diazoxide:
• Opens K+ channels & stabilizes membrane
potential
• Similar to thiazide but has no diuretic effect
• Given by IV infusion 15 mg/min until BP
controlled
V. Fenoldopam:
o Arteriolar dilator for hypertensive emergencies
o D1 agonist

34. Choice of Antihypertensive
• Hypertensive Emergencies:
– Frusemide IV, Na+ nitroprusside IV infusion,
diazoxide IV, labetalol IV
• Hypertension and Heart Failure:
– ACE (-)s, Diuretics
– CCBs are contraindicated

35. Choice of Antihypertensive
• Hypertension in Pregnancy:
– Methyldopa, β blockers, hydralazine
– ACEIs (teratogenic) & diuretics (volume depletion
are contraindicated)
• Hypertension and PVD:
– CCBs, diuretics
– β blockers are contraindicated --- vasospasms

36. Choice of Antihypertensive
• Hypertension & IHD:
– CCBs, β blockers (except in variant’s angina)
• Hypertension and Diabetes:
– ACEIs (favorable effect on sugar & lipids), Selective
α1 blockers
– β blockers & diuretics are contraindicated –
glucose intolerance

37. THX